A case of an Odontoid fracture presented to us with neurological deficit. MRI done to look for the status of cord compression revealed a concurrent vertebral artery dissection, which had been asymptomatic. There being no compressive element on the spinal cord, patient was treated conservatively. Recovery was uneventful and at eight months post injury, patient is mobilising with the use of an external brace. There is no residual effect of the arterial dissection. Review of literature on vertebral artery dissection is presented.

Introduction
Fractures of the odontoid are seen in about ten
per cent of all cases of fracture-dislocations of the cervical spine. Dissections of the vertebral artery have been noted as a rare complication following trauma to the neck. We would like to report here such a case of dissection of the extracranial part of the vertebral artery, which occurred in a case of fracture of the odontoid process. The patient was treated successfully by conservative means.

Case History
A 23 year old female presented to us with a history of fall from height with her neck in extension. She immediately had a neurological deficit which was more on one side i.e. the left. X-ray showed a minimally displaced fracture of the Odontoid process extending into the body of C2 i.e. a type 3 fracture as per the Anderson D’Alonzo classification.1 When the patient was sent for a Magnetic Resonance scanning to know the status of cord compression a startling finding was revealed: there was dissection of the right side vertebral artery. At the same time, MR Angiogram was also performed which showed the picture very clearly (Fig. 1). MR showed no compressive element; however a slight cord contusion was noted along with local cord oedema due to the odontoid fracture.

It was decided to conservatively manage the fracture with skeletal traction and Gardner-Wells tongs applied, keeping the position of extension for a period of four weeks after which tongs were removed and patient mobilized with a custom-made cervical brace with an occipitomandibular and sternal support. Neurology improved rapidly for the initial two weeks after which it was more gradual.

Fig. 1 : MRI showing vertebral artery dissection.

Follow-up so far is 32 weeks since injury. Now she has full motor power in all limbs, spasticity however being present. Current X-ray shows gradually progressing union at the fracture. No instability is noted on stress X-rays. She is doing all activities with the brace. This is to be continued till solid union at the fracture site.

Discussion
Odontoid fracture is not an uncommon pathology noted in cervical spine injuries. However, neurological deficit with such injuries is rare as compared to the incidence of deficit in other injuries of the cervical spine. This is due to the relatively larger cross sectional area of the upper cervical spinal canal. Harrop et al2 noted only 17 cases of odontoid fracture with neurological deficit among a total of 5096 cervical spinal injuries in their epidemiologial study with factors such as increased severity of trauma and male sex as predisposing to deficit. Most important was the finding in their study that anteroposterior diameter and cross-sectional area of the canal at C2 level was smaller in neurologically impaired patients, even though displacement of the fragments may not be different from those of unimpaired patients.

Extra-cranial vertebral artery injury during cervical trauma needs to be suspected not only in the case of vertebrobasilar ischaemia, but also in asymptomatic patients presenting serious flexion-distraction deformities. Fracture of the transverse foramen or facet joint dislocation should alert the clinician.3 Risk factors like sports activities, chiropractic manoeuvres and possible neck injuries have been identified. Signs on presentation4,5 included cerebellar, basilar artery and lateral medullary syndromes, visual field anomalies and decreased level of consciousness. Headache and vertigo thought to be common symptoms were actually not so. It is advisable to do vertebral angiography in suspicious cases as vertebral artery injury may be more common than suspected and may simulate traumatic brain damage. The most important factors related to an unfavourable prognosis were bilateral dissection6,7 and dissection associated with subarachnoid haemorrhage.

Fast et al8 have identified three locations where the vertebral arteries are susceptible to trauma: the transverse foraminae, atlanto-axial joint and at the occipito-atlantal joint. Because of the frequent inequality in the size of the two vertebral arteries, damage to the larger artery may lead to ischaemia of the brain stem. Shibata et al9 have reported a case of basilar artery occlusion of traumatic vertebral artery dissection managed successfully by endovascular treatment with local arterial fibrinolysis with urokinase for basilar artery occlusion and angioplasty with self expandable stent for the site of vertebral artery dissection. Important conclusions reached by Golueke et al10 are: 1) unilateral vertebral artery occlusion seldom results in a neurologic deficit if there is a normal contralateral vertebral artery and PICA (posterior inferior cerebellar artery) blood supply is preserved; 2) accurate measurement of a vertebral artery injury requires contralateral vertebral arteriogram; 3) management of vertebral artery injury is simplified by proximal, and if possible, distal therapeutic embolization; 4) an anterior approach to the C1-2 vertebral artery is a satisfactory method of obtaining distal surgical control, obviating the need to unroof the bony canal of the vertebral artery; 5) angiography is necessary in penetrating neck trauma to identify occult vascular injuries.

Referenes

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